It’s on sale for $8.99 and it’s currently only available through Amazon’s Kindle format. Even if you don’t have a Kindle devise though, you can download it onto your computer.

Thank you in advance to anyone who purchases it!

If you purchase/read it, please leave a review on Amazon. All reviews are greatly appreciated!

Spoiler – like the Floxie Hope web site, the ebook doesn’t have a cure for fluoroquinolone toxicity in it. I don’t know of a cure that has been discovered yet. It does have words of advice that I hope are helpful and inspirational though. I think/hope that it’s helpful to know that people have gotten through fluoroquinolone toxicity, and it’s good to hear about how they got through. I really do hope that it’s helpful to those who are going through fluoroquinolone toxicity! Floxies certainly need all the help and support they can get.

The more places information about fluoroquinolone toxicity can be found, the better. Now when people are searching for information about fluoroquinolone toxicity on Amazon, they can find the Floxie Hope ebook. Maybe it will help some people to put together the pieces as to why they are sick and in pain.

The ebook focuses on hope and healing. I have posted a mix of things on the Floxie Hope web site. Some of the things that I’ve posted are hopeful, but other things aren’t. This ebook focuses on the more hopeful messages.

I realize, and want to acknowledge, that not everyone recovers from fluoroquinolone toxicity. But even those whose lives are permanently changed can be helped by hearing hopeful messages.

I truly hope that the book is helpful to all who read it! Thank you to all who do!

It has recently been discovered that, “chemicals or genetic mutations that impair topoisomerases, and possibly other components of the transcription elongation machinery that interface with topoisomerases, have the potential to profoundly affect expression of long ASD (autism spectrum disorder) candidate genes.” (1)

Topoisomerases are enzymes that are essential for DNA and RNA replication and reproduction. Without topoisomerase enzymes, DNA and RNA supercoiling fail to resolve correctly during cell division and gene transcription. Topoisomerases are like oil to the DNA and RNA replication engine—making the process go smoothly. Without topoisomerases, DNA and RNA supercoiling jams up and “over-heats,” causing transcription errors. Topoisomerases are also “integral for gene expression, as they resolve DNA supercoiling that is generated during transcription.” (1)

Many pharmaceutical drugs inhibit topoisomerases. Most of these drugs are chemotherapeutic agents such as topotecan, a drug used to treat various forms of cancer. The most widely used topoisomerase inhibitors are fluoroquinolone antibiotics—Cipro/ciprofloxacin, Levaquin/levofloxacin, Avelox/moxifloxacin and Floxin/ofloxacin—drugs used to treat simple urinary tract, prostate, sinus and other infections. The fluoroquinolone antibiotics that are in wide use were first patented in the late 1980s and their use increased steadily from then until now, with 26.9 million prescriptions for orally and IV administered fluoroquinolones written in 2011. (2) A similar number of topically administered fluoroquinolone prescriptions have been written, and though orally and IV administered fluoroquinolones are not recommended for use in children because they cause cartilage lesions in juvenile animals (3), topically administered fluoroquinolones are approved for use in children as young as 6 months of age (4), and are regularly given to young children in the form of ear and eye drops.

Autism rates have been skyrocketing since the 1980s, with the most recent numbers out of the CDC stating that one in 68 American children is on the autism spectrum. (5)

It is likely that a variety of environmental and genetic components has led to the staggering figure of 1 in 68 American children on the autism spectrum. Studies have focused on vaccines (and there are vaccine injured children), but epidemiological studies have suggested that factors other than vaccines are likely at play. Birth control pills, acetaminophen, antidepressants and other categories of drugs have been pointed to for their deleterious effects on the human brain, and their possible contributions to the increasing number of people on the autism spectrum.

The mechanism of action for other fluoroquinolones—Levaquin/levofloxacin, Avelox/moxifloxacin, Floxin/ofloxacin, and their generic equivalents—are the same.

Why anyone thought that it was a good idea to give DNA disrupting chemotherapeutic drugs to children with ear infections is beyond my comprehension, but it happens every day.

Fluoroquinolone use has gone up hand in hand with autism rates. As critics of all possible causes of autism are quick to point out, correlation does not mean causation. While that criticism is true, the causes of autism are undoubtedly correlated with autism rates, and thus correlations should be examined.

The articles that I will be reviewing note that topoisomerase interrupting drugs profoundly affect the expression of genes related to autism. A large number of the genes that have been found to be related to autism are particularly long and complex, and are related to neurotransmitter synaptic function and neurodevelopment. The expression of these long genes is affected by topoisomerase interrupting drugs, as one may expect when noting that topoisomerases are necessary for gene transcription, and longer genes can more easily get mis-transcribed when exposed to topoisomerase interrupting drugs.

Topoisomerase enzymes are expressed throughout the adult brain, and thus the connections between topoisomerase inhibiting drugs and neurodegenerative diseases should be explored along with connections between those drugs and autism. It is noted in “Topoisomerases facilitate transcription of long genes linked to autism” that, “Our findings suggest that chemicals and genetic mutations that impair topoisomerases could commonly contribute to ASD and other neurodevelopmental disorders.”

It should be noted that the existing studies have looked at nuclear gene expression, and that the effects of topoisomerase interrupting drugs on the expression of mitochondrial and microbiome genes have not yet been explored.

The implications of “Topoisomerases facilitate transcription of long genes linked to autism” and “Topoisomerase 1 inhibition reversibly impairs synaptic function” are potentially huge given the wide-spread use of topoisomerase interrupting fluoroquinolones, both directly in humans and in agriculture. If fluoroquinolones are conclusively linked to autism, their use in children and people of child-bearing age (exactly how gene expression is affected by topoisomerase interrupting drugs, and what the intergenerational effects may be, are not yet known) should be prohibited—effective immediately—regardless of what the average physician who knows little about the effects of topoisomerase inhibitors on gene expression thinks about the “excellent safety record” of fluoroquinolones as a class of drugs.

As a person who has been hurt by ciprofloxacin, a fluoroquinolone antibiotic, I am not without bias—but I do not think that it’s unreasonable to assert that all topoisomerase interrupting drugs should be strictly limited—especially if they’re connected in any way to autism or neurodegenerative diseases.

STUDIES LINKING TOPOISOMERASE INTERRUPTING DRUGS TO AUTISM

“Our data suggest that chemicals or genetic mutations that impair topoisomerases, and possibly other components of the transcription elongation machinery that interface with topoisomerases, have the potential to profoundly affect expression of long ASD candidate genes. Length-dependent impairment of gene transcription, particularly in neurons and during critical periods of brain development, may thus represent a unifying cause of pathology in many individuals with ASD and other neurodevelopmental disorders.”

This conclusion has multiple levels of significance. It involves a shift in thinking about ASD as either a genetic disorder or an environmentally caused disorder, to noting the interplay between genes and the environment (epigenetics).

The study is also significant in that it notes that genes that encode synaptic function and neurodevelopment, that are also related to autism, are particularly long and complex. Those long and complex genes aren’t transcribed properly when topoisomerase enzymes are inhibited via pharmaceuticals. When topoisomerase interrupting drugs impair gene transcription, expressions of long genes become impaired.

Whether or not the silencing of expression of particularly long genes through topoisomerase interrupting drugs is a possible unifying cause of autism spectrum disorders depends on the prevalence of topoisomerase interrupting drugs in our environment. Topotecan, the topoisomerase 1 interrupter that was studied, is a chemotherapeutic drug that is only used in cancer patients, and is rarely used in pediatric patients. Fluoroquinolone antibiotics, on the other hand, are topoisomerase interrupting drugs that are used commonly in the general population, including the pediatric population, and are even used in agriculture and thus are present in the food we eat, the soil our food is grown in and even the water we drink.

More than 20 million prescriptions for fluoroquinolones—topoisomerase interrupting drugs—have been written each year for more than two decades. One is hard pressed to find an adult American who has not had at least one fluoroquinolone prescription in his or her lifetime. Fluoroquinolone use has gone up hand in hand with incidence rates of autism. As noted earlier, that correlation does not mean causation, but if topoisomerase interrupting drugs in our pharmacies and environment are a unifying cause of ASD (and other neurodegenerative diseases of modernity), fluoroquinolones would need to be the causal factor, not prudently used chemo drugs like topotecan. Studies looking into this line of thinking are pending, and the similarities between fluorquinolones and chemotherapeutic topoisomerase interrupters have not escaped the attention of the researchers looking into the relationships between topoisomerases and autism.

The UNC researchers found that, “topotecan reduced expression of nearly all extremely long genes in mouse cortical neurons,” (1) and were able to reproduce the same results in human neurons. Interestingly, not only was the expression of long genes suppressed, “topotecan increased expression of a majority of genes that were <67 kb in length, although the magnitude of this increase was very small for most genes.” (1) The expression of long genes, those genes that are involved in encoding neural synapses, was downgraded, whereas the expression of shorter genes was up-regulated.

An example of a particularly long gene that is related to ASD whose expression is altered by topotecan is “Ubiquitin-protein ligase E3A (Ube3a), a gene that affects synaptic activity and that is deleted or duplicated in distinct neurodevelopmental disorders (Angelman syndrome and autism, respectively)” (7) Ube3a is “normally expressed only from the maternal allele in neurons and regulates synaptic function.” (1) However, in cells that have been exposed to topoisomerase interrupting drugs, the paternal allele of Ube3a is transcriptionally upregulated. “Duplication of the chromosomal region containing maternal Ube3a is frequently detected in individuals with autism.”

Other particularly long genes are affected by topoisomerase interrupting drugs include:

“many genes down-regulated by topotecan are associated with synapses, cell adhesion, and neurotransmission. Moreover, a number of those down-regulated long genes are associated with autism, including Neurexin-1 (Nrxn1; 1059 kb), Neuroligin-1 (Nlgn1; 900 kb) and Contactin-associated protein 2 (Cntnap2; 2,241 kb), genes that are well known to regulate inhibitory and excitatory synaptic function.” (7)

“The quinolones are a family of broad-spectrum antibiotics. They inhibit the bacterial DNA gyrase or the topoisomerase IV enzyme, thereby inhibiting DNA replication and transcription. Eukaryotic cells do not contain DNA gyrase or topoisomerase IV, so it has been assumed that quinolones and fluoroquinolones have no effect on human cells, but they have been shown to inhibit eukaryotic DNA polymerase alpha and beta, and terminal deoxynucleotidyl transferase, affect cell cycle progression and function of lymphocytes in vitro, and cause other genotoxic effects. These agents have been associated with a diverse array of side-effects including hypoglycemia, hyperglycemia, dysglycemia, QTc prolongation, torsades des pointes, seizures, phototoxicity, tendon rupture, and pseudomembranous colitis. Cases of persistent neuropathy resulting in paresthesias, hypoaesthesias, dysesthesias, and weakness are quite common. Even more common are ruptures of the shoulder, hand, Achilles, or other tendons that require surgical repair or result in prolonged disability. Interestingly, extensive changes in gene expression were found in articular cartilage of rats receiving the quinolone antibacterial agent ofloxacin, suggesting a potential epigenetic mechanism for the arthropathy caused by these agents. It has also been documented that the incidence of hepatic and dysrhythmic cardiovascular events following use of fluoroquinolones is increased compared to controls, suggesting the possibility of persistent gene expression changes in the liver and heart.”(8)

Also, it has been known since 1996, when “Delayed Cytotoxicity and Cleavage of Mitochondrial DNA in Ciprofloxacin-Treated Mammalian Cells” was published in Molecular Pharmacology, that fluoroquinolones deplete mitochondrial DNA. The article states, “The loss in mtDNA was associated with a delayed loss in mitochondrial function. Here, we report that the 4-quinolone drug ciprofloxacin is cytotoxic to a variety of cultured mammalian cell lines at concentrations that deplete cells of mtDNA.” (9) Nuclear gene expression is linked to mitochondrial functioning and, “Mitochondria generate signals that regulate nuclear gene expression via retrograde signaling,” (10). Fluoroquinolone induced mitochondrial DNA damage may lead to changes in nuclear DNA expression.

Fluoroquinolones are also known to affect neurotransmitters, particularly GABA neurotransmitters. (11) GABA neurotransmitters are responsible for regulation of inhibitory and excitatory synaptic function. It is noted in “Topoisomerase 1 inhibition reversibly impairs synaptic function” that, “GABA-A receptor subunits are encoded by long genes.” And that, “multiple synaptic proteins encoded by long genes including cell adhesion molecules linked to autism and GABA receptor subunits, are depleted in topotecan-treated neurons.”

Given that GABA receptors are critical for inhibitory and excitatory synaptic functioning, examining the role between GABA receptors, topoisomerases, topoisomerase inhibiting drugs, and attention deficit hyperactivity disorder (ADHD) is certainly warranted. Many individuals with ASD also display symptoms of ADHD, and the interactions between GABA and glutamate receptors may be why many individuals with ASD find symptom relief through a gluten and casein free diet that is low in glutamate.

As the title of “Topoisomerase 1 inhibition reversibly impairs synaptic function” indicates, it was found that “the synaptic effects of topotecan are reversible” upon washout of the drug. However, the complexity of neurotransmission is acknowledged in the discussion section of the article, where it is noted that, “adding back one synaptic cell-adhesion molecule would not likely restore the protein levels of all affected synaptic cell-adhesion molecules as well as multiple GABA-A receptor subunits.” It is also noted that, “transient TOP1 (topoisomerase 1) inhibition has the potential to impair brain function reversibly, whereas a persistent change in TOP1 activity has the potential to disrupt neurodevelopment and promote neurodegeneration.” With limited exposure to a topoisomerase interrupting drug, the neurological effects appear to be reversible. However, persistent exposure can cause more persistent harm.

Adult patients with fluoroquinolone toxicity syndrome often note that they were able to tolerate fluoroquinolones without experiencing adverse effects prior to getting “floxed.” This tolerance threshold may indicate that fluoroquinolones somehow accumulate in cells and that the adverse effects of fluoroquinolones are amplified with each exposure. It is also possible that mitochondrial DNA needs to cross over a damage threshold before resulting in adverse effects. More about this can be found in the post, “The Fluoroquinolone Time Bomb – Answers in the Mitochondria.”

IS IT POSSIBLE THAT FLUOROQUINOLONE ANTIBIOTICS ARE RESPONSIBLE FOR MANY CASES OF AUTISM?

The possibility hasn’t been explored, despite the documented effects of fluoroquinolones that line up with many of the symptoms and effects of autism. In addition to the correlation between fluoroquinolone prescription rates and autism rates, and the points noted above about topoisomerase interrupting drugs changing the expression of autism related genes, fluoroquinolones also damage mitochondria (12)—and mitochondrial damage has been linked to autism (13) . Fluoroquinolones also cause cellular leakage (14) and depletion of minerals (15) that are necessary for synthesis of minerals and vitamins that (deficiencies of) have been linked to autism (16). Fluoroquinolones, as powerful antibiotics, are extremely destructive to the gut microbiome and gut microbiome health has also been linked to autism (17).

Even though a pretty good argument can be made for fluoroquinolones causing autism, if there is a relationship, it is not entirely clear-cut. There are children who have been hurt by fluoroquinolones, but there are also children who have been administered fluoroquinolones without any apparent harm. Like adults, children almost certainly have a tolerance threshold for fluoroquinolone use before they are injured. Delayed adverse reactions (18) make recognition of symptoms of fluoroquinolone toxicity difficult to recognize, and recognition in the pediatric population is even more difficult because children have incompletely developed communication skills. Studies that take into account delayed reactions and tolerance thresholds for fluoroquinolones have not been conducted on the adult population, much less the pediatric population, and thus it is unknown what the true effects of fluoroquinolones are.

It is possible that parental genes are altered by fluoroquinolone use and the damaged genes are passed on to children. This possibility has not yet been explored, but, anecdotally, it does not appear to be a clear-cut relationship either. Many mothers and fathers who have suffered from fluoroquinolone toxicity have had neurodevelopmentally normal children. Some have had neurodevelopmentally challenged children though too, and it would be nice to see an actual study of the children of parents exposed to fluoroquinolones, as opposed to the anecdotes that are currently available.

Autism is a complicated disorder (or set of disorders) that likely has multiple environmental, genetic and epigenetic causes. I strongly suspect that fluoroquinolones are part of the autism-cause-puzzle, but I also suspect that other cellular poisons compound the deleterious effects of fluoroquinolones on neural synapses, and can trigger autism.

I noted above that adverse reactions to fluoroquinolones are often delayed. Delayed adverse reactions to fluoroquinolones have been reportedly triggered by other stressors, including other pharmaceuticals (especially NSAIDs and steroids), benzodiazepine withdrawal, vigorous exercise, emotional stress, alcohol, hormonal changes and other things that can alter neurotransmitters and the autonomic nervous system. The combined effects of fluoroquinolones and subsequent stressors have not yet been studied, despite (some) recognition of delayed adverse reactions to fluoroquinolones.

Given the indications of “Topoisomerases facilitate transcription of long genes linked to autism,” and “Topoisomerase 1 inhibition reversibly impairs synaptic function,” it is certainly prudent to explore whether or not fluoroquinolones affect gene expression similarly to topotecan. Other drugs that inhibit topoisomerase activity, such as irinotecan and camptothecin, demonstrated similar effects to those of topotecan and thus the UNC researchers “speculate that other drugs that inhibit TOP1 or TOP2 enzymes could have similar effects on synaptic function.” We shall see if their results show that fluoroquinolones affect the expression of long genes. I’m betting that they will find that fluoroquinolones dramatically alter gene expression, especially after multiple uses and also especially when combined with NSAIDs. Given the prevalence of both fluoroquinolone antibiotics and NSAIDs in our environment though, I hope that I am wrong.

It was never prudent for fluoroquinolones to be used as first-line antibiotics. They are dangerous, DNA and RNA disrupting chemo drugs that should only be used in life-or-death situations, not as treatment for travelers’ diarrhea or sinus infections. They’re topoisomerase interrupters. They’re topoisomerase interrupters. They’re topoisomerase interrupters. They’re topoisomerase interrupters. I’m not sure how many times I need to say that for people who know what topoisomerases are (those who went to medical school) to recognize that it is NOT APPROPRIATE TO GIVE TOPOISOMERASE INTERRUPTING DRUGS TO CHILDREN (or anyone else who isn’t dying).

A former biochemist friend noted, “I was stunned that people thought quinolones were perfectly safe. Coming through the ranks, I always thought, as was taught, that they were a last-ditch drug. There was absolutely no long-term research done with them, and apparently still isn’t. But there sure was money involved.”

Long-term and intergenerational research need to be done on drugs that affect DNA before they are released into the public. Neither long-term nor intergenerational studies were done on fluoroquinolones before flooding the market with them. The odd intricacies of how fluoroquinolones affect people were not taken into consideration either—things like delayed effects, tolerance thresholds, drug and hormonal interactions, etc.

I’m hopeful that the UNC scientists that are looking at the interactions between topoisomerases and autism will start screaming about the deleterious effects of fluoroquinolones on our genes. I hope that they have the resources to do the study with delayed adverse reactions and tolerance effects taken into consideration too.

We shall see.

I’m hopeful that the study will be well-done and, if not conclusive, interesting–and that it opens the door for more research.

I can’t say that I hope that fluoroquinolones are a unifying cause of autism spectrum disorders, because that would be too sad.

One thing that I’ve found through researching how fluoroquinolones damage human health, is an appreciation for how complex and multifaceted humans are. Nothing happens in isolation. There are feedback and feedforward loops within the body that compound the effects of a stimulus on one bodily system on another, there are interactions between drugs that can occur long after a drug “should” have cleared the body, the interactions between mitochondria and neurotransmitters and cellular signaling exist but little is known about them, and more. It is difficult, if not impossible, for scientists to adequately take into account the incredible complexity of the human body. What is not known cannot be taken into consideration, and don’t for a second think that we know “enough” about the human body to be throwing pharmaceuticals that are topoisomerase interrupters into the mix.

Fluoroquinolones never should have been approved for human use until long-term, intergenerational safety studies were performed. They should be taken off of the market until those studies are done. That won’t happen though. Drugs aren’t taken off of the market unless they immediately kill a lot of people. The damage that fluoroquinolones do is more nuanced than that. If pharmaceutical makers can create a drug that is complex enough, and that can affect people in multiple different ways—through affecting gene expression—they can get away with just about anything. Bayer and Johnson & Johnson have figured this out. The FDA isn’t smart enough to protect the public. Individuals need to be smart enough to protect themselves and their families—a difficult thing to do considering that some knowledge of biochemistry and genetics is necessary for protection against dangerous pharmaceuticals.

REMAINING QUESTIONS

The existing research into connections between topoisomerase interrupting drugs and autism spectrum disorders raises multiple questions. It would be nice if some money, time, effort and other resources were devoted to answering these questions.

What are the effects of fluoroquinolone antibiotics on nuclear, mitochondrial and microbiome gene expression? What are the implications of these effects?

Do topoisomerase interrupting drugs change gene expression of the person who takes them, the offspring of the person who takes them, or both?

Do topoisomerase interrupting drugs increase a person’s chances of having a child with Autism? How?

If a person takes a topoisomerase interrupting drug, is their DNA altered? If so, are the changes temporary or permanent?

Are some people’s genes affected by these drugs more than others? What factors determine whether or not an individual’s genes are affected?

Are DNA/gene alterations triggered by pharmaceuticals reversible? If so, how?

What, if anything, can people who have taken these drugs do to discourage the expression of the ASD related genes?

When would the administration of the drug happen to influence genes in a way that could trigger the genes associated with Autism – when a mother is pregnant or at any point before the child is conceived – or does the drug need to be directly administered to the person whose genes are altered?

Do these drugs change gene expression in the ways that diet and music change gene expression or do they change DNA like Agent Orange? What level and scale are we talking about?

Several people have asked me why there aren’t more recovery stories on www.floxiehope.com. Perhaps I’m reading into the question too much, but I sense some disappointment in the question—as if the questioner believes that since there are only 37 (as of 4/23/15) stories of healing on Floxie Hope, there must only be 37 people who have recovered and everyone else must still be sick and suffering, and that’s really not very many stories and therefore most people must still be sick, and recovery is rare and everything is horrible.

I encourage you not to think those things, mainly because I don’t think they’re true.

There are many, probably thousands, of reasons why some people don’t want to share their recovery stories on Floxie Hope. Some people are too private to share things about their health on the internet. Some people feel guilty and ashamed about what they went through and don’t want their friends, family or co-workers to know that they have been dealing with health problems. Some don’t want to jinx their recovery. Some may not think that recovery from FQ toxicity is a big enough deal to write about. Some people don’t like to write. A lot of people recover from FQ toxicity without fully knowing that they were floxed – they were sick, they didn’t know why, then they got better – c’est la vie. Some people just want to forget their time of sickness and move on with their life. Some people don’t know about Floxie Hope. Some people don’t think that anyone else would be interested in their story. Some people neither like nor trust me and don’t want to contribute to my site. Some people would rather forget their time of being poisoned, and writing about it is too hard and traumatic. And there are many, many other reasons why many people who are recovered from fluoroquinolone toxicity don’t put their story up on Floxie Hope.

Please try not to read into the quantity of stories on the site, or the frequency at which recovery stories are published, as a data point about rates of recovery. I don’t think that it’s a very accurate or reliable one.

Any recovered floxies who want to write their story for Floxie Hope—I would LOVE to publish your story! Recovery stories help those who are suffering. I have received countless messages from people saying that they read the stories on Floxie Hope over and over again and that the stories of hope and recovery are what keep them going. If you can/want to give that gift to your fellow floxies, it will be greatly appreciated! Please email me any recovery stories through the Contact link on this site. Thank you!

A lot of people who have recovered from fluoroquinolone toxicity post a note about their recovery on one of the floxie facebook support groups (The Fluoroquinolone Toxicity Group – https://www.facebook.com/groups/floxies/ – is currently the biggest and most active group). Facebook is great, and there’s nothing wrong with posting a recovery story on facebook per se, my only objection to that method of conveying recovery stories is that they get lost. After a day or two, no one can find or refer back to the recovery story. The recovery post on facebook gives the people who see it hope, but it’s not available to help other people weeks, months or years down the road. Stories on web sites (Floxie Hope, or elsewhere – if you want to put it on another site, that’s cool) are stored in a single location, they’re easy for people to find, people can learn and gain from them for a long time, and the search engines can index them, raising the profile of FQ toxicity on the internet.

There’s no length or detail requirements for stories on Floxie Hope. If you want to copy your recovery blurb from facebook into an email for me to put up on the site, that can be your recovery story – no problem.

All recovery stories are GREATLY appreciated! I appreciate them and thank you in advance for your contribution to the site! Recovery stories aren’t about maintaining this site though, they’re about giving hope to your fellow floxies. Recovery stories truly do give hope, strength, and ideas for how to go about recovering to fellow floxies. Hope is immeasurably important. It’s a beautiful gift to give to others and I thank everyone who has contributed their story of hope and healing to those who are hurting – you are appreciated!

Stories about fluoroquinolone toxicity are not all recovery stories. Fluoroquinolone toxicity involves neither puppy-dogs nor sunshine. There is genuine suffering that comes before the recovery stories are possible. There are people who don’t recover. Stories of pain caused by fluoroquinolones are important and they should be shared too. I’ll write another post about the importance of sharing stories of pain caused by fluoroquinolones shortly.

Thank you to all my floxie friends who have given support, advice, and hope to their fellow floxies – especially those who have contributed (stories and comments) to this site. You are appreciated!

We all want our life to matter—to have a purpose. We all want to be valued. We all want to be seen and acknowledged. We all want to be believed. We all want our ideas to matter. We want to be listened to and heard. We all want to be respected. We all want reassurance that we matter, that we are okay and, most of all, that we are loved—unconditionally.

All of these are human desires. Everyone wants these things.

Some people are particularly good at getting these things. They are famous. They are artists—even the ones that don’t call themselves artists.

Even people who aren’t influential to thousands of other people want to be seen, acknowledged and unconditionally loved though. It’s part of being human.

People with mysterious, invisible, poorly-understood diseases often struggle with being seen and acknowledged. They are told that their disease isn’t real. They are told that they should feel fine. They are told that they are lazy or unwilling to help themselves. They are told that doctors know more about their body than they do. They are told that they are choosing to be sick. They are told that their illness is all in their head. They are told that if they only tried ___ (a new drug, diet, exercise, belief, etc.) they would be okay, and if they’re not okay after trying those things, they must not be trying hard enough.

It is mean, and cruel, to steal acknowledgement and validation from someone. It is particularly cruel to say horrible, hurtful, unacknowledging things to someone who is sick.

Who is anyone else, even a doctor, to say that your pain isn’t real? That your suffering isn’t warranted? That, because no one knows what to do to fix you, you aren’t worth fixing? That your problems and struggles are made-up choices, as opposed to “legitimate” physical health problems?

The person who is living in their body every day is more of an expert on their pain, suffering, and their disease, than ANYONE else, no matter how much schooling that person has had.

Doctors can offer insight, advice, diagnostic tools and diagnoses; they can fix many health problems, and if they’re really good a their job, they can heal people. But it really, really, really pisses me off when doctors make people who are sick and scared feel small and unworthy by not acknowledging their pain or illness.

It makes people feel small and unloved when they hear a trusted authority figure (or anyone else) says that their symptoms are imagined, or that their disease doesn’t exist.

Doctors aren’t the only people who fail to acknowledge the pain and suffering that is involved in mysterious, invisible illnesses. (Doctors are actually better, on average, about acknowledging pain and suffering than most people. It just happens to be more painful and damaging when they don’t acknowledge mysterious diseases because if they can’t even acknowledge the disease, then they can’t fix it, and if they can’t fix it, what is the sick person supposed to do??) There are a lot of people who seem to think that they’re experts on whether or not fibromyalgia, CFS/ME, fluoroquinolone toxicity, chemical sensitivities, mycotoxin/mold illness, vaccine injuries, chronic Lyme Disease, ADHD, benzodiazepine withdrawal, depression, anxiety, Morgellon’s, mitochondrial dysfunction, and other multi-symptom, mysterious, invisible, illnesses exist.

To anyone who would be so callous as to say to someone who is suffering that their disease doesn’t exist – Who are you to say, or even think, that? Who died and made you the expert on anyone else’s body? Who are you to say that you know ENOUGH about the intricacies of another person’s body to determine that YOU know what is going wrong with it?

It is ass-hole-ish and cruel dismiss people—to make them feel diminished and small. Don’t do that. It is the opposite of unconditional love. Acknowledge pain, suffering and mysterious illnesses. Acknowledge those who are going through enough crap without your judgement. It’s the right thing to do. Failing to do so makes you a jerk. Don’t be a jerk.

It is noted in the book, A Headache in the Pelvis, that, “Ciprofloxacin, one of the most powerful antibiotics, on a long-term basis proves to be only as effective as a placebo” for treatment of chronic prostatitis / chronic pelvic pain syndrome (CP/CPPS).

I just about fell out of my chair when I read that.

Ciprofloxacin, not only one of the most powerful antibiotics, but also one of the most dangerous antibiotics, is NO MORE EFFECTIVE THAN A PLACEBO for treatment of chronic prostatitis. Despite their lack of effectiveness, “Quinolones, such as ciprofloxacin, are commonly used to treat CP/CPPS because of their excellent penetration into the prostate.”

Ciprofloxacin penetrates the prostate, and every cell in the body well, but that doesn’t seem like a good enough reason to give it out to the 9-12% of men who suffer from prostatitis if it is NO MORE EFFECTIVE THAN A PLACEBO in treating chronic prostatitis.

Let’s do a cost/benefit analysis of ciprofloxacin versus a placebo.

Placebo

Benefits: Some potential alleviation of symptoms, as well as potential increases in physical and mental health scores. (The placebo effect is amazing – it’s not the same as doing nothing.)

Costs: The potential for “nocebo” effects exists – the experience of adverse effects based on the expectation of adverse effects. A placebo is a sugar pill though, and the potential for adverse effects is negligible.

Ciprofloxacin

Benefits: Some potential alleviation of symptoms, as well as potential increases in physical and mental health scores. (Same potential benefits as the placebo.)

It is criminal to subject people to a drug as dangerous as ciprofloxacin for a condition that it isn’t effective at treating. It is NOT a benign drug. It is a topoisomerase interrupter – a chemo drug – and it should NOT be used frivolously. Ciprofloxacin, and all the other fluoroquinolones, should only be used in life-threatening situations and they should NEVER be used for conditions that they are not proven effective at treating. They should NEVER be used in situations where they have been shown to be no more effective than a placebo.

This isn’t rocket science. Don’t give people dangerous drugs that don’t even have the potential for helping them. It’s not hard. But men with CP/CPPS are given ciprofloxacin, and other fluoroquinolones, as if they’re candy, to “treat” their condition. It’s absurd.

“Chronic prostatitis / chronic pelvic pain syndrome (CP/CPPS) is a common disorder and accounts for approximately 2 million visits to physicians annually in the United States. The substantial impact of CP/CPPS includes bothersome lower urinary tract symptoms, sexual dysfunction, reduced quality of life, and increased health care expenditures. The syndrome is diagnosed only on the basis of symptoms, principally pain or discomfort in the pelvis region. No objective measures can help define the disease. Although bacteria can infect the prostate, most men with prostatitis have a negative midstream urine culture, indicating that bacteria may not be the cause of their symptoms.”

“Because the cause of CP/CPPS is unknown, affected men receive many empirical therapies. The 2 most common treatments prescribed by physicians are antimicrobial agents and a-adrenergic receptor antagonists, although there is little objective evidence to support their use. Quinolones, such as ciprofloxacin, are commonly used to treat CP/CPPS because of their excellent penetration into the prostate and broad spectrum coverage for uropathogens and other organisms traditionally believed to be associated with the syndrome.”

After completing a randomized, double-blind trial on men suffering from CP/CPPS, and comparing those who received ciprofloxacin, tamsulosin, a combination of both ciprofloxacin and tamsulosin, and a placebo, it was concluded that, “Ciprofloxacin and tamsulosin did not substantially reduce symptoms in men with long-standing CP/CPPS who had at least moderate symptoms.”

Ciprofloxacin, and other antibiotics, are given to men with non-bacterial prostatitis for no good reason whatsoever. They are often given long courses as well – 6 to 12 weeks of the drugs. That’s a long enough course for many of the men who are given these drugs to cross their tolerance threshold for the drugs and get floxed.

If ciprofloxacin was effective at treating CP/CPPS, perhaps it would be worth the risk of getting floxed. But ciprofloxacin isn’t effective at treating CP/CPPS. It’s no more effective than a sugar pill and it is beyond ridiculous and wrong to expose men to a dangerous drug that doesn’t even help them.

Many symptoms of CP/CPPS, and other pelvic pain syndromes, react well to relaxation training and appear to be a response to stress and anxiety. “Chronic pelvic pain reflects tension in the pelvic floor, initiated or exacerbated by cycles of mental tension, anxiety and stress.” Pelvic pain syndromes are no more a choice than other bodily manifestations of stress such as heart attacks, back pain or tension headaches. The pain is real and it is not “in the patient’s head.” The brain is not separate from the body though, and what is going on in the head can have bodily manifestations.

The effects of ciprofloxacin, and other fluoroquinolones, on neurotransmitters may exacerbate CP/CPPS and other diseases related to stress and anxiety. Fluoroquinolones block GABA-A receptors. GABA receptors are the neurotransmitters that induce a calming response. When GABA receptors are blocked by fluoroquinolones, anxiety, insomnia, fearfulness, loss of confidence, loss of self, psychiatric illness and even seizures can result. Floxed patients often report being unable to relax, a reduced threshold for stress, autonomic nervous system dysfunction, and other symptoms of GABA neurotransmitter dysfunction. Fluoroquinolones activate the sympathetic nervous system and disrupt the balance between the sympathetic and parasympathetic nervous systems.

If CP/CPPS is primarily a response to anxiety, stress and disregulation of the sympathetic/parasympthetic nervous systems, ciprofloxacin may not only fail to improve chronic pelvic pain conditions, it may exacerbate them.

Prescribing ciprofloxacin, or any other fluoroquinolone, to patients with chronic pain and non-bacterial prostatitis, is not only not helpful – IT IS HARMFUL, and may exacerbate the condition it is prescribed to treat.

Post-script note – Many people, especially elderly women, are given fluoroquinolones to treat asymptomatic urinary tract infections after a urinalysis shows bacteria in their urine. It has recently been noted that URINE ISN’T STERILE. And again, people are getting floxed for no good reason.